Much evidence suggests that tissue damage in systemic lupus is caused by the deposition of immune complexes in tissues, followed by inflammation. We have in the past shown, in human lupus, a defect in the ability of the reticulo-endothelial system (RES) to remove particulate immune complexes (antibody-coated red cells) from the circulation. To determine whether simple overload of receptor for immunoglobulin in the RES might be responsible, capacity of circulatory RES cells - perhipheral blood monocytes - to bind immunoglobulins was measured. Contrary to expectation, the capacity was increased in patients with lupus, and the increase was correlated with disease activity, thus ruling out simple overload as an explanation for the earlier observed RES failure.